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Article ; Online: Sequencing of genes of drug response in tumor DNA and implications for precision medicine in cancer patients.

Gillis, Nancy / Etheridge, Amy S / Patil, Sushant A / Hayes, D Neil / Hayward, Michele C / Auman, J Todd / Parker, Joel S / Innocenti, Federico

The pharmacogenomics journal

2023 Volume 23, Issue 4, Page(s) 73–81

Abstract: Tumor DNA sequencing is becoming standard-of-care for patient treatment decisions. We evaluated genotype concordance between tumor DNA and genomic DNA from blood and catalogued functional effects of somatic mutations in 21 drug response genes in 752 ... ...

Abstract	Tumor DNA sequencing is becoming standard-of-care for patient treatment decisions. We evaluated genotype concordance between tumor DNA and genomic DNA from blood and catalogued functional effects of somatic mutations in 21 drug response genes in 752 solid tumor patients. Using a threshold of 10% difference between tumor and blood DNA variant allele fraction (VAF), concordance for heterogenous genotype calls was 78% and increased to 97.5% using a 30% VAF threshold. Somatic mutations were observed in all 21 drug response genes, and 44% of patients had at least one somatic mutation in these genes. In tumor DNA, eight patients had a frameshift mutation in CYP2C8, which metabolizes taxanes. Overall, somatic copy number losses were more frequent than gains, including for CYP2C19 and CYP2D6 which had the most frequent copy number losses. However, copy number gains in TPMT were more than four times as common as losses. Seven % of patients had copy number gains in ABCB1, a multidrug resistance transporter of anti-cancer agents. These results demonstrate tumor-only DNA sequencing might not be reliable to call germline genotypes of drug response variants.
MeSH term(s)	Humans ; Precision Medicine ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; DNA ; Genotype ; Sequence Analysis, DNA ; Mutation/genetics ; High-Throughput Nucleotide Sequencing ; DNA Copy Number Variations/genetics
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2023-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2106831-8
ISSN	1473-1150 ; 1470-269X
ISSN (online)	1473-1150
ISSN	1470-269X
DOI	10.1038/s41397-023-00299-7
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Article ; Online: Gene therapy: Have the risks associated with viral vectors been solved?

Auman, J Todd

Current opinion in molecular therapeutics

2010 Volume 12, Issue 6, Page(s) 637–638

Abstract: Gene therapy has the potential to cure monogenic diseases through the replacement of the deleterious gene with a functional copy. While the field of gene therapy has been plagued by serious adverse events associated with therapy, it is hoped that new, ... ...

Abstract	Gene therapy has the potential to cure monogenic diseases through the replacement of the deleterious gene with a functional copy. While the field of gene therapy has been plagued by serious adverse events associated with therapy, it is hoped that new, safer viral vectors have reduced these risks greatly. However, recently published reports indicate that these new viral vectors are a potential risk to patients receiving gene therapy. Thus, caution is required when recruiting patients for clinical trials of gene therapies to ensure the benefit of the therapy outweighs the risks.
MeSH term(s)	Genetic Therapy/methods ; Genetic Therapy/trends ; Genetic Vectors/genetics ; Humans ; Risk Assessment ; Risk Factors ; Viruses/genetics
Language	English
Publishing date	2010-12
Publishing country	England
Document type	Editorial
ZDB-ID	2022273-7
ISSN	2040-3445 ; 1464-8431
ISSN (online)	2040-3445
ISSN	1464-8431
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Article ; Online: Cancer pharmacogenomics: do cancer cell lines have the right stuff?

Auman, J Todd

Pharmacogenomics

2010 Volume 11, Issue 8, Page(s) 1035–1037

MeSH term(s)	Cell Line, Tumor ; Gene Expression Profiling ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Pharmacogenetics/methods ; Precision Medicine
Language	English
Publishing date	2010-08
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural
ZDB-ID	2019513-8
ISSN	1744-8042 ; 1462-2416
ISSN (online)	1744-8042
ISSN	1462-2416
DOI	10.2217/pgs.10.107
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Article: Adopting Duplex Sequencing™ Technology for Genetic Toxicity Testing: A Proof-of-Concept Mutagenesis Experiment with N-Ethyl-N-Nitrosourea (ENU)-Exposed Rats.

Smith-Roe, Stephanie L / Hobbs, Cheryl A / Hull, Victoria / Auman, J Todd / Recio, Leslie / Streicker, Michael A / Rivas, Miriam V / Pratt, Gabriel A / Lo, Fang Yin / Higgins, Jacob E / Schmidt, Elizabeth K / Williams, Lindsey N / Nachmanson, Daniela / Valentine, Charles C / Salk, Jesse J / Witt, Kristine L

bioRxiv : the preprint server for biology

2023

Abstract: Duplex sequencing (DuplexSeq) is an error-corrected next-generation sequencing (ecNGS) method in which molecular barcodes informatically link PCR-copies back to their source DNA strands, enabling computational removal of errors by comparing grouped ... ...

Abstract	Duplex sequencing (DuplexSeq) is an error-corrected next-generation sequencing (ecNGS) method in which molecular barcodes informatically link PCR-copies back to their source DNA strands, enabling computational removal of errors by comparing grouped strand sequencing reads. The resulting background of less than one artifactual mutation per 10 Highlights: DuplexSeq is an ultra-accurate NGS technology that directly quantifies mutationsENU-dependent mutagenesis was detected 24 h post-exposure in proliferative tissuesMultiple tissues exhibited the canonical ENU mutation spectrum 7 d after exposureResults obtained with DuplexSeq were highly concordant between laboratoriesThe Rat-50 Mutagenesis Assay is promising for applications in genetic toxicology.
Language	English
Publishing date	2023-05-09
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.08.539833
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Article: Applications of genomic tools to colorectal cancer therapeutics.

Auman, J Todd / McLeod, Howard L

Current opinion in molecular therapeutics

2008 Volume 10, Issue 6, Page(s) 548–554

Abstract: Clinically and histopathologically similar colorectal cancers exhibit considerable variability in their responses to chemotherapeutics. The advent of genomic technologies has enabled the unbiased determination of changes in DNA and RNA, alterations that ... ...

Abstract	Clinically and histopathologically similar colorectal cancers exhibit considerable variability in their responses to chemotherapeutics. The advent of genomic technologies has enabled the unbiased determination of changes in DNA and RNA, alterations that may be responsible for, or predictive of the variability in response to chemotherapy. This review highlights several advances made in applying genomic tools toward colorectal cancer therapeutics. Progress has been made using gene expression profiling to identify which colorectal cancer patients would benefit most from adjuvant chemotherapy. In addition, advances have been made in colorectal cancer pharmacogenomics by identifying gene expression patterns associated with sensitivity to specific chemotherapeutic agents. Lastly, the use of genome-wide mutation screening of individual tumor samples to identify the profiles of mutated genes is explored. Future research toward integrating genomic information with clinical and histopathological data is expected to lead to improved therapeutic management of colorectal cancer.
MeSH term(s)	Colorectal Neoplasms/genetics ; Colorectal Neoplasms/therapy ; Gene Expression Profiling ; Genome, Human ; Genomics/methods ; Humans ; Pharmacogenetics
Language	English
Publishing date	2008-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2022273-7
ISSN	1464-8431
ISSN	1464-8431
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Article ; Online: Cancer pharmacogenomics: DNA genotyping and gene expression profiling to identify molecular determinants of chemosensitivity.

Auman, J Todd / McLeod, Howard L

Drug metabolism reviews

2007 Volume 40, Issue 2, Page(s) 303–315

Abstract: Cancer patients exhibit a wide heterogeneity in their responses to chemotherapy. Improvement in chemotherapeutic responses could be achieved by gaining more detailed information on the molecular determinants (i.e., DNA, RNA or protein) underlying this ... ...

Abstract	Cancer patients exhibit a wide heterogeneity in their responses to chemotherapy. Improvement in chemotherapeutic responses could be achieved by gaining more detailed information on the molecular determinants (i.e., DNA, RNA or protein) underlying this heterogeneity. Pharmacogenomics approaches can be used to integrate information on drug responsiveness with alterations in molecular entities, often on a genome-wide scale. By using information gleaned from pharmacogenomics studies, it is anticipated that cancer chemotherapy can be tailored to the individual patient or tumor phenotype. This review focuses on pharmacogenomics studies conducted to gain insight into the molecular determinants of chemosensitivity to cancer chemotherapeutics.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genotype ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Oligonucleotide Array Sequence Analysis ; Patient Selection ; Pharmacogenetics/methods ; Phenotype ; Polymorphism, Genetic
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2007-10-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	184967-0
ISSN	1097-9883 ; 0360-2532 ; 0012-6594
ISSN (online)	1097-9883
ISSN	0360-2532 ; 0012-6594
DOI	10.1080/03602530801952427
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Article ; Online: Race does not explain genetic heterogeneity in pharmacogenomic pathways.

Yen-Revollo, Jane L / Auman, J Todd / McLeod, Howard L

Pharmacogenomics

2008 Volume 9, Issue 11, Page(s) 1639–1645

Abstract: Introduction: Polymorphic alleles in the human genome have been identified as affecting numerous drug responses. Currently, genotyping of all patients before starting a drug regimen is impractical. Since many polymorphisms occur at varying rates in ... ...

Abstract	Introduction: Polymorphic alleles in the human genome have been identified as affecting numerous drug responses. Currently, genotyping of all patients before starting a drug regimen is impractical. Since many polymorphisms occur at varying rates in different racial groups, we investigated whether a patient's race could predict presence of drug-relevant genetic variants well enough to be used as a substitute for individual genotyping. Methods: We performed hierarchical clustering and principal components analysis on tagSNPs from three pathways (irinotecan, 5-fluorouracil and insulin) across 270 individuals from four racial groups available from the International HapMap Project. Results: For the drug pathways, irinotecan and 5-fluorouracil, individuals from each race were widely dispersed, although several subclusters consisted entirely of individuals from a single racial group. Principal components analysis confirmed race was not a major contributor to the SNP data variance. Interestingly, individuals tended to cluster more by race across the endogenous insulin signaling pathway SNPs. Conclusions: Most genetic variation was determined by individual variation, not racial grouping, indicating race is not adequate as a surrogate to individualized therapy.
MeSH term(s)	Camptothecin/analogs & derivatives ; Camptothecin/pharmacokinetics ; Camptothecin/pharmacology ; Cluster Analysis ; Continental Population Groups/genetics ; Databases, Genetic ; Fluorouracil/pharmacokinetics ; Fluorouracil/pharmacology ; Genetic Heterogeneity ; Humans ; Insulin/pharmacokinetics ; Insulin/pharmacology ; Irinotecan ; Metabolic Clearance Rate ; Pharmacogenetics/methods ; Pharmacogenetics/statistics & numerical data ; Polymorphism, Single Nucleotide ; Principal Component Analysis
Chemical Substances	Insulin ; Irinotecan (7673326042) ; Fluorouracil (U3P01618RT) ; Camptothecin (XT3Z54Z28A)
Language	English
Publishing date	2008-11-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2019513-8
ISSN	1744-8042 ; 1462-2416
ISSN (online)	1744-8042
ISSN	1462-2416
DOI	10.2217/14622416.9.11.1639
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Article: Ontogenesis of beta-adrenoceptor signaling: implications for perinatal physiology and for fetal effects of tocolytic drugs.

Slotkin, Theodore A / Auman, J Todd / Seidler, Frederic J

The Journal of pharmacology and experimental therapeutics

2003 Volume 306, Issue 1, Page(s) 1–7

Abstract: G-Protein-coupled receptors play an instrumental role in cellular development and function. In the mature organism, receptor signaling is controlled through the processes of desensitization and down-regulation. Recent evidence suggests that these ... ...

Abstract	G-Protein-coupled receptors play an instrumental role in cellular development and function. In the mature organism, receptor signaling is controlled through the processes of desensitization and down-regulation. Recent evidence suggests that these regulatory mechanisms are not inherent properties, however, but rather are acquired during ontogenesis. This review focuses on beta-adrenoceptors (betaARs), which are found in fetal and neonatal tissues and are effectively linked through adenylyl cyclase (AC) to the production of cAMP. Agonist-induced stimulation of betaARs in the immature organism fails to produce desensitization, and instead, responsiveness increases. The unique mechanisms underlying this anomalous response involve induction of AC, a switch to more catalytically efficient AC isoforms, an increase in the ratio of stimulatory to inhibitory G-proteins, and interference with the expression and/or function of other G-protein-linked receptors that provide offsetting, inhibitory inputs. These adjustments are thus heterologous, influencing signaling mediated by a host of other G-protein-coupled neurotransmitter and hormone receptors. The net effect is to maintain and augment betaAR signaling in the face of continued stimulation, properties that disappear with maturation. The unique regulatory mechanisms for betaAR signaling in the fetus and neonate provide the necessary physiological adjustments required for the perinatal transition from intrauterine to extrauterine life. At the same time, however, the inability to restrict betaAR function may underlie adverse effects of betaAR-agonist tocolytics that are used in the treatment of preterm labor.
MeSH term(s)	Adrenergic beta-Agonists/pharmacology ; Animals ; Fetus/drug effects ; Fetus/physiology ; Humans ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Tocolytic Agents/pharmacology
Chemical Substances	Adrenergic beta-Agonists ; Receptors, Adrenergic, beta ; Tocolytic Agents
Language	English
Publishing date	2003-07
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.102.048421
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Article ; Online: Genetic variation determines VEGF-A plasma levels in cancer patients.

Scientific reports

2018 Volume 8, Issue 1, Page(s) 16332

Abstract: Angiogenesis is essential in tumor biology and is regulated by vascular endothelial growth factor (VEGF) ligands and receptors. Here we aimed to discover genetic variants associated with levels of circulating angiogenic proteins in cancer patients. ... ...

Abstract	Angiogenesis is essential in tumor biology and is regulated by vascular endothelial growth factor (VEGF) ligands and receptors. Here we aimed to discover genetic variants associated with levels of circulating angiogenic proteins in cancer patients. Plasma was collected at baseline in 216 pancreatic and 114 colorectal cancer patients. Thirty-one angiogenic proteins were measured by ELISA. 484,523 Single Nucleotide Polymorphisms (SNP) were tested for association with plasma levels for each protein in pancreatic cancer patients. Three top-ranked hits were then genotyped in colorectal cancer patients, where associations with the same proteins were measured. The results demonstrated rs2284284 and MCP1 (P-value = 6.7e-08), rs7504372 and VEGF-C (P-value = 9.8e-09), and rs7767396 and VEGF-A (P-value = 5.8e-09) were SNP-protein pairs identified in pancreatic cancer patients. In colorectal cancer patients, only rs7767396 (A > G) and VEGF-A was validated (P-value = 5.18e-05). The AA genotype of rs7767396 exhibited 2.04-2.3 and 2.7-3.4-fold higher VEGF-A levels than those with AG and GG genotypes. The G allele of rs7767396 reduces binding of the NF-AT1 transcription factor. In conclusion, a common genetic variant predicts the plasma levels of VEGF-A in cancer patients through altered binding of NF-AT1.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Colorectal Neoplasms/blood ; Colorectal Neoplasms/blood supply ; Colorectal Neoplasms/genetics ; Female ; Humans ; Male ; Middle Aged ; NFATC Transcription Factors/metabolism ; Neovascularization, Pathologic/metabolism ; Polymorphism, Single Nucleotide ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Vascular Endothelial Growth Factor A/blood ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; Young Adult
Chemical Substances	NFATC Transcription Factors ; RNA, Messenger ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2018-11-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-34506-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Heat map visualization of high-density clinical chemistry data.

Auman, J Todd / Boorman, Gary A / Wilson, Ralph E / Travlos, Gregory S / Paules, Richard S

Physiological genomics

2007 Volume 31, Issue 2, Page(s) 352–356

Abstract: Clinical chemistry data are routinely generated as part of preclinical animal toxicity studies and human clinical studies. With large-scale studies involving hundreds or even thousands of samples in multiple treatment groups, it is currently difficult to ...

Abstract	Clinical chemistry data are routinely generated as part of preclinical animal toxicity studies and human clinical studies. With large-scale studies involving hundreds or even thousands of samples in multiple treatment groups, it is currently difficult to interpret the resulting complex, high-density clinical chemistry data. Accordingly, we conducted this study to investigate methods for easy visualization of complex, high-density data. Clinical chemistry data were obtained from male rats each treated with one of eight different acute hepatotoxicants from a large-scale toxicogenomics study. The raw data underwent a Z-score transformation comparing each individual animal's clinical chemistry values to that of reference controls from all eight studies and then were visualized in a single graphic using a heat map. The utility of using a heat map to visualize high-density clinical chemistry data was explored by clustering changes in clinical chemistry values for >400 animals. A clear distinction was observed in animals displaying hepatotoxicity from those that did not. Additionally, while animals experiencing hepatotoxicity showed many similarities in the observed clinical chemistry alterations, distinct differences were noted in the heat map profile for the different compounds. Using a heat map to visualize complex, high-density clinical chemistry data in a single graphic facilitates the identification of previously unrecognized trends. This method is simple to implement and maintains the biological integrity of the data. The value of this clinical chemistry data transformation and visualization will manifest itself through integration with other high-density data, such as genomics data, to study physiology at the systems level.
MeSH term(s)	Animals ; Chemical and Drug Induced Liver Injury/blood ; Clinical Chemistry Tests ; Cluster Analysis ; Color ; Computer Graphics ; Liver Function Tests ; Male ; Rats ; Rats, Inbred F344
Language	English
Publishing date	2007-07-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2038823-8
ISSN	1531-2267 ; 1094-8341
ISSN (online)	1531-2267
ISSN	1094-8341
DOI	10.1152/physiolgenomics.00276.2006
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